PULMONOLOGY: Anatomy&Physiology: Dr.

Esguerra  Density: (not uniform)

o Near hilum: 1g/ml
T1.1 Components of the Normal Human Lung o Peripheral: 0.1g/ml
Component Volume or Mass (mL) Thickness o Density is not uniform  will contribute to the differences
(m) in the ventilation & perfusion ratio
Gas 2400  Blood vessels:
o More distended at base
Tissue 900
o Increasing vascular distending pressure- 1cmH20/cm
- Blood 400 down height
- Lung 500 o Blood vessels are usually more concentrated & more
^ Support strucs 250 concentrated on lung bases this is the reason why most
^ Alveolar walls 250-300 of the blood flow & most of the air flow goes to the base
^ Epithelium 60-80 0.18 of the lung
^ Endothelium 50-70 0.10 o Usually because the blood vessels becomes less as it
^ Interstitium 100-185 0.22 goes up the lung, & as the blood vessels becomes less
distended as you go up the lung, the blood as well as
^ Alveolar m 55
the air flow decreases as you go from the base of the
In a normal lung, most of its components are made up of gas
lung as you go up to the lung (apex of the lung)
 Around 2400 ml
o In early cases of pulmonary edema or pulmonary
 Mostly nitrogen then oxygen congestion, one of the earliest changes that you could
see in Xray would be abundancy of the blood vessels in
Gross organization of human lung the upper lung fields
o The main reason why more blood vessels are distended
 Img: Midfrontal section-cadaveric thorax
in the base of the lung is because of gravity although
 Img: CXR lung at FRC (AP-Lat)
there are also other non-gravitational factors
Gross & subgross characteristics
Interstitial connective tissue compartments (CT):
 Weight: 900-1000g
 Parenchymal (alveolar) interstitium
o 40-50% blood
 Loose-binding connective tissue (extra-alveolar)
o Adult lung weighs 900-1000g
o Peribronchovascular sheath
o >50%: air
o Interlobular septa
o 40-50% blood (BV, lymphatics)
o Visceral pleura
 Gas volume:
 *Bulk of interstitium: ground substance or GAG matrix
o End expiration: 2.5L
o Max inspiration: 6L
Lung Embryology
 2 distinct embryologic origins:
Precursors of the different parts of the lung (upper & lower
airways particularly the larynx, esophagus, trachea, lung
parenchyma)
o Primitive foregut endoderm
o Lateral mesoderm
 Above are embryologic precursors of:
o Larynx
o Esophagus
o Tracheobronchial tree
o Lung parenchyma

Stages of lung development

1. Embryonic Period
 1st 8 wks after fertilization
 Lung appears at 26th day of gestation as ventral diverticulum of
the foregut
 Becomes prominent w/ formation of laryngo-tracheal groove
 Lung bud invades splanchnic mesoderm
 Divides into 5 saccules (L-2; R-3)
 Lobar bronchi formed by 37th day
 Segmental bronchi at 41st day

 1st sign of lung development – LUNG BUD (appears at the 26th

week of gestation)
 Lung bud will develop into saccules (2 on the left, 3 on the
right) & will later develop into major lobar bronch:i
o 2 on the left – upper, lower( lingular segment is
considered the middle segment of the left),
o 3 on the right – upper, middle, lower
2. Pseudoglandular Stage
 5-17 wks of gestation
 Formation of 20 (of 24) airway generations, lined by columnar
epithelial cells
 Ciliated, goblet, basal cells appear in central airways
 Cartilage & smooth muscles formed in trachea
 Vascular system develops along bronchial tree
 Bochdalek hernia (*pl)
 Major development that occurs in this stage is the
development of airway generation
 The different bronchi will now develop during the
pseudoglandular stage  bronchioles or the smaller bronchi
 If the mother of the baby becomes sick, or taking drugs that
are contraindicated during pregnancy during this age of
gestation  may develop DIAPHRAGMATIC
HERNIA/BOCHDALEK HERNIA
3. Canalicular Stage
 16-26th wks
 Characterized by appearance of pulmonary acinus, abundant
capillaries, & progressive differentiation of airway epthelial cells
 Marginal gas exchange capability (survival possible)
 Surfactant synthesis & secretion
 During the first few stages (mother delivers the baby), the baby
will die because there is no lung function, still no gas exchange.
 This is the stage where in the lung is capable of minimal gas
exchange. Some babies delivered 25-26 wks may survive
although they may develop respiratory distress syndrome
because the gas exchange is still minimal aside from the fact
that surfactant synthesis & secretion only starts at this time
 Babies delivered prematurely will develop neonatal respiratory
distress syndrome mainly because of ↓ in surfactant production.

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  PURPOSE OF SURFACTANT: ↓ the surface tension so when the
baby is delivered the lungs would expand
 ↑ surface tension – lung would not expand, lung is not
compliant
4. Saccular Stage
 24-40 wks
 Peripheral airways form widened airspaces or saccules giving
rise to alveolar ducts & sacs
 When the baby is delivered at this time, the baby may survive &
may not even develop respiratory distress
5. Alveolar Stage
 36 wks-18th postnatal months
 Bulk of alveolar formation occurs postnatally
 Saccules become alveolar sacs
 50M alveoli (newborn lungs)
 300M alveoli (adult lung)
 last of the intrauterine development
 In this stage you will know how many alveoli will be in the adult
lung.
6. Microvascular Stage
 Postnatal development
 Transformation of the structures of interalveolar walls
 Double-layered capillary system of interalveolar septa is
completely restructured into single intraseptal network
 Usual development: Neurovascular system

Upper Airways:
MAIN PURPOSE OF THE UPPER AIRWAY – Conduction of gases, no gas exchange occurs, found the majority of the dead space

o LOC, increases angle

Nasal Cavity o Extend head & jaw to form straight tube
 Gateway to the respiratory system
o Alae (rubbery entry ways) Larynx
o Vestibules (space on each side)  Sound production
o Conchae (bony plates each side of vestibule)  Protective valve:
o Nasal septum (divides nasal cavity, extends o Adam’s apple or laryngeal prominence (midline of
posteriorly) thyroid cartilage)
 Warm & humidify air (moisture comes from mucus produced by o Vocal cords
submucosal glands & goblet cells) o Cricoid cartilage
 ALAR FLARING – one of the earliest signs that the baby is having  Below thyroid cartilage
respiratory distress  Complete ring of hyaline cartilage
 May also trap airway molecules  Emergency tracheostomy
 Transtracheal aspiration
Mucosal lining:  When you press the adam’s apple- like pressing the voice box
 Squamous mucosa  the voice will change
o Mouth  ACUTE LARYNGITIS – manifest with hoarseness
o Pharynx
o Larynx
 Tall columnar ciliated epithelium Trachea
o Nasal cavities  Extends through into the mediastinum up to the middle 3rd of
o Sinuses sternum
o Trachea  2-2.5cm diameter & 11cm long
o Conduction airways  16-20 U shaped cartilages, 0.4-0.5cm high
 Posterior w/ thin muscle btwn open ends of the U.
Oral Cavity  Support yet allows some variation in diameter during expiration
 Accessory airway passage & coughing
 Warms incoming air  Air filled structure
 Saliva wets & provides moisture for inhaled air  Main upper airway
 Tongue  Hollow musclular tube, cartilagenous tube
o Deglutition & speech
 The reason why this does not collapse during inspiration &
o Taste buds
expiration would be the 16-20 U shaped cartilages
o Nerve endings (protective gag reflex)
 It also humidifies mainly because of saliva o Compliant because of the cartilages
 LARYNX – main organ for phonation  C shaped cartilages: protection at the front rather than at the
posterior ???
 TONGUE – Will also prevent aspiration
 (+) Phlegm  deep cough  trachea will collapse a liitle 
expel the phlegm in your lungs ( it would not collapse totally
Pharynx because of its C shaped cartilages)
 Space behind nasal cavity & mouth  Part of the conducting airways, still no gas exchange occurs at
 Extends where the larynx & esophagus separate this area
o Nasopharynx (shut off during swallowing)
o Oropharynx (opens during swallowing)

 When the nasopharynx does not close, some of the food

particles will go to the trachea or the airway. Sometimes when
the patient is swallowing, the nasopharynx is still open, that’s
the time the patient may manifest with incessant coughing until
the food particles is expelled out of the lungs (unless the food
particles are large).

Epiglottis
 Extends from the base of the tongue
 2-4cm long, 0.2-0.5cm thick
 Guards against aspiration
 Flap valve over the entry to the larynx
o Closes on swallowing
o Alteration of coordination with other NM reflexes
o Cough reflex as back-up
 Head & airways- 90 degree angle

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Airways
Airway Generations  Cross section of the lungs  no cartilages  level of membranous
bronchioles (usually non-cartilagenous)

1. Bronchi
 Cartilagenous walls

2. Membranous bronchioles
 Noncartilagenous, 1mm diameter or less
 Numerous but short
 Tightly embedded in CT framework, therefore
 Enlarge passively as lung volume increases


3. Respiratory bronchioles or gas exchange ducts or alveolar ducts

 Serve dual function (airway & gas exchange)
 Do not contribute to anatomic dead space
 Conduct air from the membranous bronchioles going to the
alveolar duct or alveolar sac. As early as the respiratory
bronchioles there is already gas exchange but majority occurs
at alveolar ducts or alveolar sac
 It will conduct air towards the most distal part of the airway.
EXTRA PULMONARY – outside the lung parenchyma  Serves as gas exchange in the airway ????
INTRA PULMONARY – inside the lung parenchyma
The conducting zones
 Total volume: 150 ml
 Respiratory bronchioles: part of the gas exchange unit. Not a part of
o 50% in URT
the conducting airways
o 50% in LRT (up to terminal bronchioles)
 Bronchi & Membranous bronchioles: part of the intrapulmonary  Anatomic dead space
airways, but they are still part of the conducting airways o Upper (extrapulmo) & cartilaginous airways
 No gas exchange!

 Gas flow is through convection or bulk flow

 From nasal cavity to membranous brochioles
 Only function is to conduct air
.
 DEAD SPACE : volume or amount of air that does not
participate in the gas exchange
Upper (extrapulmonary) airways  Majority of the dead space is found in the conducting airways
 Bronchomotor tone:partial constriction  BULK FLOW : pressure volume will push the air towards the lower
 Most airway resistance part of the airways.
 There is still dead space when you reach the alveoli???
Lower (intrapulmonary) airways: Upper airways up to the level of the
bronchi: still have cartilages.

Anatomy of Respiratory Tract
(The Bronchopulmonary Segments)

Right lung Left lung
Upper lobe Upper
 Apical  Apico-posterior
 Posterior  Anterior
 Anterior  Superior lingula
Middle lobe  Inferior lingula
 Lateral Lower
 Medial  Superior
Lower lobe  Antero-medial
 Superior  Lateral
 Medial  Posterior
 Anterior
 Lateral
 Posterior
 RIGHT LUNG: Right upper lobe bronchi will supply the right upper lobe segment
o Usually there are 3 main lobes (upper, middle, lower)
o As far as segments are concerned, there are 10 anatomic segment in the right lung
 LEFT LUNG: divided into upper & lower lobe (there is no middle lobe)
o Lingular segment is like a middle lobe but still part of the upper lobe. Corresponds to the middle lobe of the right lung.
o There are 8 segments in the left lung

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Bronchopulmonary Segments:
 (+) foreign body aspiration  will lodge in the right lung because it is shorter &more straight from the trachea
 It is difficult to extract foreign body in the left lung & treat aspiration pneumonia because it is not straight & has an acute angle
 Very important in Xray findings because certain pneumonias or diseases only occupy certain parts of the segments of the lung
 TUBERCULOSIS – usually on the apicoposterior
 ASPIRATION – lower lobes (anterior segment)
 If the patient is in supine position, possible aspiration in the posterior segment of the upper lobes

Schematic representation of anatomic relationship: 
pleura, diaphragm, mediastinum, lung

Cellular complexity of the airways

1. Epithelial Cells  Tone altered by
 Nearly half are ciliated (down to bronchioles) o ANS/mediators from effector cells
 Majority of the epithelial cells are ciliated up to the part of the o Forced expiration & coughing
bronchioles  Smooth muscle cells are usually affected during asthmatic
attacks, bronchoconstriction in cases of COPD.
2. Cilia  Tone altered by ANS mediators esp histamine & serotonin
 6 um in length, 0.3 um in width
 Motile cilia is arranged longitudinally, in microtubular doublets 9. Mast Cells
 Motility rests on sliding movements of microtubules  Release mediators that may affect smooth muscles stimulate
 Cilia move the superficial liquid lining layer towards the pharynx mucus production & induce mucosal edema by increasing
from deep within (centripetal) permeability of vessels
 Disappears in respiratory bronchioles  cellular components that contain inflammatory mediators.
 Main purpose of the cilia is for motility, mucus extraction. Mainly  usually seen but are not granulated
mucociliary transport  In the presence of basophils in cases of hyperasthma, they can
 Only found at the level of the membranous bronchioles & become degranulated releasing inflammatory mediators
usually disappear at the level of respiratory bronchioles particularly histamine & serotonin that would stimulate smooth
muscle contraction, mucus secretion. This is why in patients with
3. Apical Junctional Complexes asthma, once you stimulate the mast cells, there is airway
 Between airway epithelial cells narrowing mainly because of smooth muscle contraction that is
 Impt. For metabolically regulated secretion & absorption of aggravated by excess mucus production
electrolytes & water from liquid lining
o Zonula occludens 10. Clara cells
 Restricts diffusion  Primary site of xenobiotic metabolism, affected by cytochrome
 Polarizes cellular functions between P450 monooxygenase system (metabolizes carcinogens &
apical& baso-lateral membranes toxicants)
o Zonula adherens  Source of apoproteins assoc. with surface active materials
o Macula adherens  Synthesis, secretion, & storage of lipids and glycoproteins
 We don’t easily develop pulmonary edema because of the  Progenitors of ciliated and new clara cells
zonula occludens (Restricts diffusion of any type of molecule  Site of xenobiotic metabolism: metabolism of inhaled
either air or fluid) carcinogens or the inhaled drugs or inhaled toxic agents would
 In patients with pulmonary edema or ARDS in adults, one of the occur
problem is in the zonula occludens  It could also be a source of apoproteins which is also needed in
the production of the surfactant
4. Glands  It could also be a precursor cell or progenitor cells of ciliated
 Found in submucosa of cartilaginous bronchi, none in and new clara cells
membranous bronchi
 Secretes water, electrolytes & mucin into lumen
 Release modulated by neurotransmitters, inflammatory
mediators
 In asthma, once the Basophils & mast cells are granulated 
would stimulate the secretion of mucus into the lumen 
mucus plugging and hyperemia in patients with asthma (these
glands once stimulated by different neurotransmitters
particularly histamine & serotonin)

5. Goblet Cells
 Mucin secreting epithelial cells
 Decreases in number peripherally, normally disappearing in
terminal bronchioles

6. Basal cells
 Along basal lamina of airways
 Precursor cells for other epithelial cells including ciliated cells
 when epithelial cells are destroyed, basal cells will become
precursor cells for the formation of other epithelial cells or
ciliated cells

7. Lymphocytes
 Intercalated between airway epithelial cells
 Cytotoxic lymphocytes undergo IgA class antibody response
 T & B cells in lamina propia beneath airway epithelium
 BALT- principally B cells, express IgA
 A reminder that lung is in constant challenge with airborne
immunologic stimuli
 Lymphocytes are for immune function
 Epithelial cells are usually IgA in response

8. Smooth Muscle Cells

 Extends as far as respiratory bronchioles

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Circulation
The bronchial circulation (systemic) T1.2 Quantitative Data on Intrapulmonary Blood Vessels in Humans
Bronchial artery
 Branch out from aorta or upper intercostal artery Vessel Class Diameter Volume (mL) Surface Area
 0.5-1.5% of cardiac output (w/dm) (m2)
 Blood supply to: Arteries >500 m 68 0.4
o trachea (& esophagus)
Arterioles 13-500 m 18 1.0
o Mainstem bronchi
Capillaries 10m 60-200 50-70
o Pulmonary vessels into the lungs
o Visceral pleura, interlobular septa Venules 13-500 m 13 1.2
o Airways down to & including terminal bronchioles Veins >500 m 58 0.1
 Pulmonary artery & bronchial artery – dual circulation
 Majority of the nutrients that is delivered in the lungs is delivered Pulmonary Circulation Functions:
by the BRONCHIAL ARTERY 1. Gas exchange
2. Capacitance reservoir between the right & left side of the
heart
Venous drainage 3. Blood filter
 Bronchial veins to azygos & hemiazygos veins RA 4. Endothelial cells:
 Bronchial blood Pulmonary veins LA (venous admixture) a. Inactivation of angiotensin, bradykinins & PGE1
b. Endothelium dependent vasoactivity
Clinical significance of bronchial circulation:
 mainly gas exchange. Oxygen coming from the alveoli will go to the
Bronchial artery supplies the ffg: pulmonary circulation. Excess carbon dioxide coming from the body
1. Long standing inflammatory & proliferative diseases such as  pulmonary circulation  alveoli  carbon dioxide is exhaled.
carcinoma, bronchiectasis.
2. Scar tissue
 Primary source of new blood vessels after lung injury (enormous
growth potential)
 Usually feeds carcinoma cells
 Carcinoma & bronchiectasis - one of the manifestations is
hemoptysis.
o And one of the treatment in hemoptysis whether carcinoma or
bronchiectasis is BRONCHIAL ARTERY EMBOLIZATION (blockage
of bronchial artery)

The pulmonary circulation

 Pulmonary artery:
o Enters the lung at the hilum
o Travels adjacent to & branches with each airway
generation down to respiratory bronchioles
o Pressure varies by about 24cmH2O over the full
length of the lung
 Low pressure or resistance circulation (1/10th of systemic)
 Under normal conditions, blood volume in pulmonary capillaries
is well below its maximal capacity
 The pulmonary circulation
 Small pulmonary arteries supplies a specific volume of
respiratory tissue, veins drains portions of several such zones
 Most blood volume is in the large vessels, all surface area is in
smaller vessels
 Vasoactive regulation plays a role in the local regulation of
blood flow in relation of ventilation
 Pulmonary veins follow Miller’s dictum (as far away from the
airways as possible)
 Respond to different drugs

Miller’s dictum
 Bronchial arteries descend along posterior aspect of bronchi
distally to respiratory bronchioles
 Pulmonary veins, at base of bronchopulmonary segments, are
found in interlobular septae w/lymphatics
o Typically, as far away from centrilobular bronchioles
as possble

Pulmonary blood vessels: 2 groups

Alveolar vessels
 Within alveolar walls
 Embedded in parenchymal connective tissue
 Affected by alveolar pressure

Extra-alveolar vessels
 Lying in loose-binding connective tissue (peribronchovascular
sheath, interlobular septa)

Intrapulmonary blood vessels

Terminal respiratory unit (TRU)

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  All alveolar ducts, together with all accompanying alveoli that
stem from most proximal respi bronchiole Alveolar epithelium: 
The pneumocytes
 Both anatomic & functional existence TYPE I TYPE II
 100 alveolar ducts & 2000 alveoli  90-95% of alveolar surface  Small, cuboidal
 5 mm in diameter with a volume of 0.02ml (at FRC) area  Proliferate in cases of injury:
 Shape maintained at FRC & TLC, distorted at low vol  Large, thin flat cells o Give rise to new
 150,000 TRU’s in human lungs  Membranous cells type II cells & new
o ACINUS: 10-12 TRU  Fragile and easily injured type I
Cells of TRU predom capillary endothelium of pulmo circ :  Specialized for gas  Cell of origin of surfactant
1. Type I flat alveolar cells exchange  Synthetic, secretory, repair
2. Type II granular pneumocyte  Incapable of cell division factories
3. Alveolar macrophages

Alveolus
 Complex geometric structure with flat walls and sharp
curvature at the junctions between adjacent walls (not
spherical)
 Most distal lung unit
 Site of gas exchange
o RB, alveolar ducts, alveolar ducts & sacs, & alveoli
o Flow is primarily diffusion starting from generation 17-19
 Resting volume of alveolus: 10-14% of TLC
 Alveolar walls are composed primarily of pulmonary capillaries
Lung units and their connections

Lobules  Two groups:

 Has small veins and outline polygonal units o 1. Superficial plexus - Connective tissue of visceral
 3-8 centrally placed terminal bronchioles and accompanying pleura
arteries o 2. Deep plexus - Peribronchovascular sheath
 Blood enters the lobule centrally and empties on the sides Note:
 Infections, hemorrhage and aspiration respect these 1. Communication exist between plexuses (bidirectional flow of
boundaries lymph)
2. Centripetal flow toward hilum or pulmonary ligament (to
Interconnections regional LN)
1. Pores of Kohn 3. No lymphatics in the alveolar walls
 Between alveolar septa
 5-15 um in diameter
 Explains the partially aerated lung tissue beyond a completely (+) Problem in the alveolar walls  what drains the fluid are the alveolar
obstructed bronchus macrophages
2. Interlobular fissures

Innervation
AFFERENT pathways
 Sensory pathway
 Myelinated stretch (hering-breuer reflex) & irritant receptors
 Most are non-myelinated C fibers (sense parenchymal tissue
distortion, congestion and interstitial edema)
 Travel in the vagus nerve and terminate in vagal nuclei in the
medulla oblongata
 Respiratory center: pons and medulla

EFFERENT pathways
 Motor pathway
 Reach the lung through sympathetic (T1-4/5 ganglia) and
parasympathetic (brainstem motor nuclei associated with
vagus nerve) nervous system
 Pain innervation is mostly in the parietal pleura

APUD
 Amine precursor uptake and decarboxylase system
(neuroendocrine system)
 Composed of:
o neuroendocrine cells
o neuroepithelial bodies
 Distributed on the airway epithelium to alveolar ducts
 Neuroepithelial bodies are preferentially located at airway
bifurcations

 Storage site of
o Amine hormones (Serotonin, Dopamine, NE)
o Peptide hormones (Bombesin, Calcitonin, Leu-
enkephalin)
 ROLE: Release hormones that affect smooth muscles and
hence may act as peripheral chemoreceptors (hypercapnea
and acute alveolar hypoxia)

Lymphatic system
 Extensive lymphatic system
 Function:
o Liquid homeostasis
o Respiratory defense mechanism

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